Expression and distribution of symplekin regulates the assembly and function of the epithelial tight junction

The epithelial tight junction (TJ) was first described ultrastructurally as a fusion of the outer lipid leaflets of the adjoining cell membrane bilayers (hemifusion). The discovery of an increasing number of integral TJ and TJ-associated proteins has eclipsed the original lipid-based model with the wide acceptance of a protein-centric model for the TJ. In this review, we stress the importance of lipids in TJ structure and function. A lipid-protein hybrid model accommodates a large body of information supporting the lipidic characteristics of the TJ, harmonizes with the accumulating evidence supporting the TJ as an assembly of lipid rafts, and focuses on an important, but relatively unexplored, field of lipid-protein interactions in the morphology, physiology, and pathophysiology of the TJ.

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Microtubules are required for efficient epithelial tight junction homeostasis and restoration

AJP Cell Physiology ◽

10.1152/ajpcell.00336.2013 ◽

2014 ◽

Vol 307 (3) ◽

pp. C245-C254 ◽

Cited By ~ 25

Author(s):

Lila G. Glotfelty ◽

Anita Zahs ◽

Catalin Iancu ◽

Le Shen ◽

Gail A. Hecht

Keyword(s):

Tight Junction ◽

Vital Role ◽

Structure And Function ◽

Paracellular Transport ◽

Microtubule Disruption ◽

Junction Protein ◽

Epithelial Tight Junction ◽

And Function ◽

Junction Structure

Epithelial tight junctions are critical for creating a barrier yet allowing paracellular transport. Although it is well established that the actin cytoskeleton is critical for preserving the dynamic organization of the tight junction and maintaining normal tight junction protein recycling, contributions of microtubules to tight junction organization and function remain undefined. The aim of this study is to determine the role of microtubules in tight junction homeostasis and restoration. Our data demonstrate that occludin traffics on microtubules and that microtubule disruption perturbs tight junction structure and function. Microtubules are also shown to be required for restoring barrier function following Ca2+ chelation and repletion. These processes are mediated by proteins participating in microtubule minus-end-directed trafficking but not plus-end-directed trafficking. These studies show that microtubules participate in the preservation of epithelial tight junction structure and function and play a vital role in tight junction restoration, thus expanding our understanding of the regulation of tight junction physiology.

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First Encounter: How Pathogens Compromise Epithelial Transport

Physiology ◽

10.1152/physiol.00015.2004 ◽

2004 ◽

Vol 19 (5) ◽

pp. 240-244 ◽

Cited By ~ 16

Author(s):

Karl Kunzelmann ◽

Brendan McMorran

Keyword(s):

Ion Channels ◽

Tight Junction ◽

Signaling Pathways ◽

Epithelial Transport ◽

Structure And Function ◽

Electrolyte Transport ◽

Physiological Functions ◽

Epithelial Tight Junction ◽

And Function ◽

Do So

Pathogenic organisms trigger numerous signaling pathways that ultimately lead to drastic changes in physiological functions. Apart from altering structure and function of the epithelial tight junction barrier and activating inflammatory cascades, they induce changes in fluid and electrolyte transport. Pathogens do so by activating or by inhibiting ion channels and transporters, and the result might be to their benefit or to their disadvantage.

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